PT - JOURNAL ARTICLE AU - FABIOLA SESTI AU - OURANIA E. TSITSILONIS AU - ATHANASSIOS KOTSINAS AU - IOANNIS P. TROUGAKOS TI - Oxidative Stress-mediated Biomolecular Damage and Inflammation in Tumorigenesis DP - 2012 May 01 TA - In Vivo PG - 395--402 VI - 26 IP - 3 4099 - http://iv.iiarjournals.org/content/26/3/395.short 4100 - http://iv.iiarjournals.org/content/26/3/395.full SO - In Vivo2012 May 01; 26 AB - At the cellular level, free radicals are tightly controlled by an inducible antioxidant program, since at low non-hazardous amounts they contribute to physiological signalling and homeostasis. However, high levels of oxidative stress promote the accumulation of damaged biomolecules, the impairment of cell signalling pathways and the increase of oncogenic hits. As the intracellular and extracellular levels of oxidative stress increase during ageing or in various diseases, so does the amount of damaged biomolecules, since the repair mechanisms are also targets of oxidative damage and thus become gradually ineffective over time. Depending on the severity of the biomolecular damage, the responses of normal human cells to oxidants may range from transient growth arrest to premature senescence, and even to cell death. Although some responses are clearly tumour suppressing (apoptosis), others may be potentially oncogenic as they combine damage accumulation with a retained ability for proliferation (transient growth arrest) or with inflammation (senescence, necrosis). This array of events significantly increases the likelihood of the appearance of tumour-initiating cells, which may then give rise to pre-neoplastic focal lesions and eventually to neoplasia. In the present manuscript, we will focus on the role of free radical-mediated biomolecular damage and inflammation in tumorigenesis.